The role of APOE gene polymorphisms in lung adenocarcinoma susceptibility and lipid profile

BackgroundAPOE gene polym orphisms have been linked to Alzheimer’s disease and coronary heart diseases. However, their relationship with lung adenocarcinoma (LUAD) remains uncertain.MethodsThis study analyzed a cohort of 600 individuals comprising 200 LUAD patients in the lung cancer group and 400 h...

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Main Authors: Huanhuan Bi, Dunqiang Ren, Ye Wang, Hongmei Wang, Chunling Zhang
Format: Article
Language:English
Published: Frontiers Media S.A. 2024-12-01
Series:Frontiers in Immunology
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Online Access:https://www.frontiersin.org/articles/10.3389/fimmu.2024.1522761/full
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author Huanhuan Bi
Dunqiang Ren
Ye Wang
Hongmei Wang
Chunling Zhang
author_facet Huanhuan Bi
Dunqiang Ren
Ye Wang
Hongmei Wang
Chunling Zhang
author_sort Huanhuan Bi
collection DOAJ
description BackgroundAPOE gene polym orphisms have been linked to Alzheimer’s disease and coronary heart diseases. However, their relationship with lung adenocarcinoma (LUAD) remains uncertain.MethodsThis study analyzed a cohort of 600 individuals comprising 200 LUAD patients in the lung cancer group and 400 healthy individuals as controls. APOE gene variants were identified through Sanger sequencing. Statistical analyses were conducted to assess intergroup differences, and comparisons of lipid profiles were performed across individuals carrying different APOE alleles.ResultsThe APOE ϵ2 allele had been significantly more frequently occurring in the LUAD group than in the control group (15.5% vs. 7%, P <0.001). APOE ϵ2/ϵ2 and ϵ2/ϵ3 genotypes increased susceptibility to LUAD by 3.78-fold and 3.22-fold. The APOE ϵ2/ϵ3 genotype increased the risk of early-stage LUAD by 2.36-fold and advanced-stage LUAD by 4.05-fold. Individuals with the APOE ϵ2/ϵ2 genotype had a 3.22-fold higher susceptibility to moderately differentiated and a 6.8-fold higher susceptibility to poorly differentiated LUAD. Patients with the ϵ2 allele in LUAD exhibited disrupted lipid metabolism, characterized by reduced HDL, TC, and FFA levels, along with increased ApoB, particularly in advanced and poorly differentiated cancer stages.ConclusionIndividuals carrying the ϵ2 allele have an increased susceptibility to developing LUAD, accompanied by disrupted lipid metabolism. Additionally, the APOE ϵ2/ϵ2 and ϵ2/ϵ3 genotypes are associated with an increased risk of developing advanced and poorly differentiated LUAD.
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spelling doaj-art-9549771ef98f478494885117be9876212025-08-20T02:40:22ZengFrontiers Media S.A.Frontiers in Immunology1664-32242024-12-011510.3389/fimmu.2024.15227611522761The role of APOE gene polymorphisms in lung adenocarcinoma susceptibility and lipid profileHuanhuan Bi0Dunqiang Ren1Ye Wang2Hongmei Wang3Chunling Zhang4Department of Respiratory and Critical Care Medicine, School of Medicine, Qingdao University, Qingdao, ChinaDepartment of Respiratory and Critical Care Medicine, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, ChinaClinical Laboratory, Qingdao Central Hospital, University of Health and Rehabilitation Sciences, Qingdao, Shandong, ChinaDepartment of Respiratory and Critical Care Medicine, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, ChinaDepartment of Respiratory and Critical Care Medicine, Qingdao Central Hospital, University of Health and Rehabilitation Sciences, Qingdao, Shandong, ChinaBackgroundAPOE gene polym orphisms have been linked to Alzheimer’s disease and coronary heart diseases. However, their relationship with lung adenocarcinoma (LUAD) remains uncertain.MethodsThis study analyzed a cohort of 600 individuals comprising 200 LUAD patients in the lung cancer group and 400 healthy individuals as controls. APOE gene variants were identified through Sanger sequencing. Statistical analyses were conducted to assess intergroup differences, and comparisons of lipid profiles were performed across individuals carrying different APOE alleles.ResultsThe APOE ϵ2 allele had been significantly more frequently occurring in the LUAD group than in the control group (15.5% vs. 7%, P <0.001). APOE ϵ2/ϵ2 and ϵ2/ϵ3 genotypes increased susceptibility to LUAD by 3.78-fold and 3.22-fold. The APOE ϵ2/ϵ3 genotype increased the risk of early-stage LUAD by 2.36-fold and advanced-stage LUAD by 4.05-fold. Individuals with the APOE ϵ2/ϵ2 genotype had a 3.22-fold higher susceptibility to moderately differentiated and a 6.8-fold higher susceptibility to poorly differentiated LUAD. Patients with the ϵ2 allele in LUAD exhibited disrupted lipid metabolism, characterized by reduced HDL, TC, and FFA levels, along with increased ApoB, particularly in advanced and poorly differentiated cancer stages.ConclusionIndividuals carrying the ϵ2 allele have an increased susceptibility to developing LUAD, accompanied by disrupted lipid metabolism. Additionally, the APOE ϵ2/ϵ2 and ϵ2/ϵ3 genotypes are associated with an increased risk of developing advanced and poorly differentiated LUAD.https://www.frontiersin.org/articles/10.3389/fimmu.2024.1522761/fullAPOEgene polymorphismslung adenocarcinomalipid metabolismtotal cholesterol
spellingShingle Huanhuan Bi
Dunqiang Ren
Ye Wang
Hongmei Wang
Chunling Zhang
The role of APOE gene polymorphisms in lung adenocarcinoma susceptibility and lipid profile
Frontiers in Immunology
APOE
gene polymorphisms
lung adenocarcinoma
lipid metabolism
total cholesterol
title The role of APOE gene polymorphisms in lung adenocarcinoma susceptibility and lipid profile
title_full The role of APOE gene polymorphisms in lung adenocarcinoma susceptibility and lipid profile
title_fullStr The role of APOE gene polymorphisms in lung adenocarcinoma susceptibility and lipid profile
title_full_unstemmed The role of APOE gene polymorphisms in lung adenocarcinoma susceptibility and lipid profile
title_short The role of APOE gene polymorphisms in lung adenocarcinoma susceptibility and lipid profile
title_sort role of apoe gene polymorphisms in lung adenocarcinoma susceptibility and lipid profile
topic APOE
gene polymorphisms
lung adenocarcinoma
lipid metabolism
total cholesterol
url https://www.frontiersin.org/articles/10.3389/fimmu.2024.1522761/full
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